The purpose of this study is to examine the effect of a pharmacologically induced deficiency in glutamatergic transmission at the N-methyl-D-aspartate (NMDA) receptors on amphetamine induced dopamine (DA) release in humans. The hypothesis that schizophrenia might be associated with a deficiency in NMDA transmission will be further explored, and this investigation may better elucidate the bridge between DA and glutamate hypotheses of schizophrenia.